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Induction of fibroblast‐like cells from CD34 + progenitor cells of the bone marrow in rheumatoid arthritis
Author(s) -
Hirohata Shunsei,
Yanagida Tamiko,
Nagai Tatsuo,
Sawada Tetsuji,
Nakamura Hiroshi,
Yoshino Shin’ichi,
Tomita Tetsuya,
Ochi Takahiro
Publication year - 2001
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.70.3.413
Subject(s) - cd34 , bone marrow , fibroblast , progenitor cell , biology , immunology , tumor necrosis factor alpha , stem cell , cancer research , microbiology and biotechnology , cell culture , genetics
To assess the role of bone marrow in the pathogenesis of rheumatoid arthritis (RA), we examined the capacity of CD34 + cells from bone marrow to generate fibroblast‐like type B synoviocytes. CD34 + cells from the bone marrow of 22 RA patients differentiated into cells with fibroblast‐like morphology, which expressed prolyl 4‐hydroxylase, in the presence of stem cell factor (SCF), granulocyte‐macrophage colony‐stimulating factor (GM‐CSF), and tumor necrosis factor α (TNF‐α), much more effectively than CD34 + cells from bone marrow of 15 control subjects (10 patients with osteoarthritis and 5 healthy individuals). The generation of fibroblast‐like cells was not at all observed in cultures with SCF, GM‐CSF, and interleukin 4 (IL‐4) with or without TNF‐α. Generation of fibroblast‐like cells was correlated with matrix metalloproteinase (MMP)‐1 levels in culture supernatants. Thus, MMP‐1 levels were significantly higher in TNF‐α‐stimulated cultures of bone marrow CD34 + cells from patients with RA than in those from the control group. These results indicate that bone marrow CD34 + cells from patients with RA have abnormal capacities to respond to TNF‐α and to differentiate into fibroblast‐like cells producing MMP‐1, suggesting that bone marrow CD34 + progenitor cells might generate type B synoviocytes and thus could play an important role in the pathogenesis of RA.